Evidence map›Paper›PMID 28575082›Full record

ArticlePloS one2017

The role of reactive oxygen intermediates in the intracellular fate of Leptospira interrogans in the macrophages of different hosts.

Shijun Li, Peili Li, Lei Zhang, Weilin Hu, Ming Wang, Ying Liu, Guangpeng Tang, Dingming Wang, Bijun Zhou, Jie Yan

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.2field-weighted citation impact, top 25% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Infection and immunity · 2022
    Article
  3. Article
  4. Leptospirosis and Coinfection: Should We Be Concerned?International journal of environmental research and public health · 2021
    Review
  5. Article
  6. Article
  7. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 1 country.

Shijun LiInstitute of Communicable Disease Control and Prevention, Guizhou Provincial Center for Disease Control and Prevention, Guiyang, Guizhou, P.R. China.ORCID http://orcid.org/0000-0002-4677-6301
Peili LiCollege of Animal Science, Guizhou University, Huaxi District, Guiyang, Guizhou, P.R. China.
Lei ZhangZhejiang Provincial Center for Disease Control and Prevention, Hangzhou, Zhejiang, P.R. China.
Weilin HuDepartment of Medical Microbiology and Parasitology, College of Medicine, Zhejiang University, Hangzhou, P.R. China.
Ming WangCollege of Animal Science, Guizhou University, Huaxi District, Guiyang, Guizhou, P.R. China.
Ying LiuInstitute of Communicable Disease Control and Prevention, Guizhou Provincial Center for Disease Control and Prevention, Guiyang, Guizhou, P.R. China.
Guangpeng TangInstitute of Communicable Disease Control and Prevention, Guizhou Provincial Center for Disease Control and Prevention, Guiyang, Guizhou, P.R. China.
Dingming WangInstitute of Communicable Disease Control and Prevention, Guizhou Provincial Center for Disease Control and Prevention, Guiyang, Guizhou, P.R. China.
Bijun ZhouCollege of Animal Science, Guizhou University, Huaxi District, Guiyang, Guizhou, P.R. China.
Jie YanDepartment of Medical Microbiology and Parasitology, College of Medicine, Zhejiang University, Hangzhou, P.R. China.
Guizhou Center for Disease Control and Prevention · CNGuizhou University · CNZhejiang University · CNZhejiang Center for Disease Control and Prevention · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPathogenic species of Leptospira cause leptospirosis, a global zoonotic disease. Our previous work showed that leptospires survive and replicate in human macrophages but are killed in murine macrophages. However, the mechanism responsible for the different intracellular fates of leptospires within the macrophages of different hosts remains unclear.

resultsThe present study demonstrates that infection with Leptospira interrogans caused significant up-regulation of reactive oxygen species (ROS) and superoxide in J774A.1 cells but did so to a lesser extent in THP-1 cells. The up-regulation of ROS and superoxide was significantly inhibited by the NADPH oxidase inhibitor apocynin. The damaged leptospires and remnants of leptospires within membrane-bound vacuoles were significantly inhibited by apocynin in J774A.1 cells but were less inhibited in THP-1 cells. In addition, apocynin significantly prevented damage to leptospires and the co-localization of L. interrogans with lysosomes in J774A.1 cells but did so to a lesser extent in THP-1 cells. Furthermore, the relative fluorescence intensity levels of intracellular leptospires and the viability of the intracellular leptospires increased in apocynin pretreated J774A.1 and THP-1 cells after 2 h of infection.

conclusionsThe present study, based on our previous findings, further demonstrated that ROS contributed substantially to the bactericidal ability of mouse macrophages to kill intracellular leptospires. However, ROS did not contribute as much in human macrophages, which partially explains the different intracellular fates of L. interrogans in human and mouse macrophages.

Indexed as

AnimalsCell LineHost-Pathogen InteractionsHumansLeptospira interrogansMacrophagesMiceReactive Oxygen SpeciesReactive Oxygen Species

Identifiers

PMID28575082
PMCPMC5456347
OpenAlexW2621131950

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.